Proteolysis of the lung has been proposed as a pathogenic mechanism in chronic obstructive lung disease and it has been demonstrated that proteolytic enzymes from several sources can produce lung lesions in experimental animals similar to human emphysema. Cigarette smoking causes a marked increase in alveolar macrophage proteolytic enzymes but does not increase intraalveolar alpha 1-antitrypsin levels. The objective of this study would be to measure proteolytic enzymes and inhibitors in the alveolar spaces of patients with chronic obstructive lung disease. Surgically resected lungs will be lavaged and elastase, neutral and acid protease, and alpha 1-antitrypsin levels will be determined on cell and fluid fractions of the lavage. Inhibition of these enzymes by alpha 1-antitrypsin and concentrated lavage fluid will be measured. Enzyme activity and inhibitor levels will be correlated to smoking history, pulmonary function abnormality, and histology of resected lung specimen.